Posted on 31 July 2020
At the very start of the pandemic, scientists across the world scrambled to make sense of the limited data that was available at the time. While many aspects of thisremain mysterious, our understanding of Sars-CoV-2 has increased massively, and it’s not surprising that many of our initial ideas about the disease have changed. Here are 5 things we have learned about COVID-19:
When COVID-19 first began to find its way across the world at the start of the year, health workers knew to watch for three symptoms: fever, cough, and shortness of breath. Since then, the list of Covid symptoms has been expanded significantly. The peculiar loss of smell and taste emerged as a prominent symptom, so much so that it is now grounds for self-isolation and seeking a test. Others experienced headaches, rashes, swelling, diarrhoea or, more commonly, no symptoms at all.
Bizarre symptoms continue to emerge even now, such as ”COVID toes”, a painful or itchy rash that sometimes occurs in mildly affected or otherwise asymptomatic young adults.
Why are Covid’s symptoms so disparate? We still don’t know for certain, but there’s been recent speculation that the circulatory system may be involved. Blood clots are occurring frequently enough in COVID-19 cases for clinicians to take notice: Growing evidence suggest that SARS-CoV-2 can infect endothelial cells in the walls of blood vessels, which might disrupt the way blood flow and clotting are regulated.
Sars-CoV-2 infects human cells by binding to the ACE2 receptors, which are found on cells in the nose, throat and lungs. But these receptors are also present in other organs, including the heart and gut. As case numbers climbed we soon realised that COVID-19, was not ‘just a respiratory disease’, and frequently damages other organs as well: kidney stress and failure, liver injury, brain damage and most of all, heart failure.
In April, Susan Parson, MD, a Bay Area medical examiner, made the startling discovery that one of the first people in the U.S. to die from COVID-19 had died not of can participate) is currently underway to better understand the effects of Covid on the heart. It is possible that some people could be suffering from the cardiovascular effects of COVID-19, but not the respiratory and other symptoms. This is concerning – the focus on respiratory symptoms may mean we are missing a large number of cases., but from a ruptured heart. We now know that existing heart conditions are a huge risk factor for death from COVID-19, and a study (called COVID-19 Citizen Science, in which anyone with a smartphone
When studies showed that the virus could survive for days on certain surfaces, there was concern that Covid could be spread on letters, packages and door handles. It doesn’t hurt to be cautious, but there’s currently no solid evidence that infection regularly occurs in this way. We now believe that the majority of transmission happens during close contact with others, with the highest risk of infection in enclosed, crowded environments.
One of the very first things we heard about the novel coronavirus was that it mainly killed the elderly. Early data from Wuhan gave hope that deaths among young people and children were nonexistent or extremely rare. While it remains true that this age group is highly protected against COVID-19, it is clear that children and young people are less safe than originally thought. Children can experience a rare but serious inflammatory reaction called “multisystem inflammatory syndrome in children”. This can cause rashes, fever, diarrhea and even.
Young people with other medical conditions are more likely to die from severe Covid, but it is entirely possible for healthy individuals to succumb as well. These people are statistical outliers, but they exist, and understanding what makes them different may help us understand how the disease functions. Some have speculated that differences in ACE2 expression, or genetic mutations that affect the immune system, may help explain why some young people respond so badly to infection.
COVID-19 usually doesn’t feel anything like a. Fewer than 20% of infected people who come to a hospital say they have experienced a sore throat or runny nose. Fevers, dry coughs and loss of sense of smell or taste appear to be far more common sympoms during the first few days of an infection, assuming you have symptoms to begin with.
One of the stranger findings concerning Sars-CoV-2 is that it is not very cytopathic – that is to say, theitself often doesn’t kill the cells that it infects. Comparatively, is far deadlier to human cells. It is the overreaction of the immune system that causes most of the organ damage associated with Covid, and ultimately seems to be what kills the host.
There are two arms of the immune system. Theimmune system can mount a response tailored to the individual pathogen it is fighting, and can also form an immune memory to quickly respond if the pathogen is ever encountered again. The other arm of the immune system – the innate immune system – is capable of responding to any pathogen, and is mainly responsible for causing inflammation.
Inflammation causes blood vessels toand become more permeable, allowing more to access the site of infection. However, this also allows fluid to enter the lungs, making breathing difficult. Furthermore, an extreme inflammatory response can lead to inflammation occurring throughout the body. When inflammation is localised to one place, it usually serves to help the immune system fight an infection. However, when inflammation occurs throughout the body, the result is catastrophic, leading to life-threatening low blood pressure (septic ) and multiple organ failure. For many COVID-19 patients, this is the cause of death.
That concludes our list of ways our understanding of COVID-19 has improved. This list will no doubt continue to grow as our knowledge of thecontinues to evolve.
We Thought It Was Just a Respiratory Virus: https://www.ucsf.edu/magazine/covid-body
Why Do Young, Healthy People Die from COVID-19?: http://protomag.com/articles/why-do-young-healthy-people-die-covid-19
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